TAILIEUCHUNG - Chapter 035. Hypoxia and Cyanosis (Part 1)

Harrison's Internal Medicine Chapter 35. Hypoxia and Cyanosis HYPOXIA The fundamental task of the cardiorespiratory system is to deliver O 2 (and substrates) to the cells and to remove CO2 (and other metabolic products) from them. Proper maintenance of this function depends on intact cardiovascular and respiratory systems, an adequate number of red blood cells and hemoglobin, and a supply of inspired gas containing adequate O2. Effects Decreased O2 availability to cells results in an inhibition of the respiratory chain and increased anaerobic glycolysis. This switch from aerobic to anaerobic metabolism, Pasteur's effect, maintains some, albeit markedly reduced, adenosine triphosphate. | Chapter 035. Hypoxia and Cyanosis Part 1 Harrison s Internal Medicine Chapter 35. Hypoxia and Cyanosis HYPOXIA The fundamental task of the cardiorespiratory system is to deliver O2 and substrates to the cells and to remove CO2 and other metabolic products from them. Proper maintenance of this function depends on intact cardiovascular and respiratory systems an adequate number of red blood cells and hemoglobin and a supply of inspired gas containing adequate O2. Effects Decreased O2 availability to cells results in an inhibition of the respiratory chain and increased anaerobic glycolysis. This switch from aerobic to anaerobic metabolism Pasteur s effect maintains some albeit markedly reduced adenosine triphosphate ATP production. In severe hypoxia when ATP production is inadequate to meet the energy requirements of ionic and osmotic equilibrium cell membrane depolarization leads to uncontrolled Ca2 influx and activation of Camdependent phospholipases and proteases. These events in turn cause cell swelling and ultimately cell necrosis. The adaptations to hypoxia are mediated in part by the upregulation of genes encoding a variety of proteins including glycolytic enzymes such as phosphoglycerate kinase and phosphofructokinase as well as the glucose transporters Glut-1 and Glut-2 and by growth factors such as vascular endothelial growth factor VEGF and erythropoietin which enhance erythrocyte production. During hypoxia systemic arterioles dilate at least in part by opening of Katp channels in vascular smooth-muscle cells due to the hypoxia-induced reduction in ATP concentration. By contrast in pulmonary vascular smoothmuscle cells inhibition of K channels causes depolarization which in turn activates voltage-gated Ca2 channels raising the cytosolic Ca2 and causing smooth-muscle cell contraction. Hypoxia-induced pulmonary arterial constriction shunts blood away from poorly ventilated toward better-ventilated portions of the lung however it also increases pulmonary .

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